Heavy Metals
Although there is
no clear definition of what a heavy metal is, density is in most cases taken to
be the defining factor. Heavy metals are commonly defined as those having a
specific density of more than 5 g/cm3. Heavy metals have been used
in many different areas for thousands of years. Lead has been used for at least
5000 years, early applications including building materials, pigments for
glazing ceramics, and pipes for transporting water. In ancient Rome, lead
acetate was used to sweeten old wine, and some Romans might have consumed as
much as a gram of lead a day. Mercury was allegedly used by the Romans as a
salve to alleviate teething pain in infants, and was later (from the 1300s to
the late 1800s) employed as a remedy for syphilis. Claude Monet used cadmium
pigments extensively in mid 1800s, but the scarcity of the metal limited the
use in artists’ materials until the early 1900s.
Although several
adverse health effects of heavy metals have been known for a long time,
exposure to heavy metals continues, and is even increasing in some parts of the
world, in particular in less developed countries, though emissions have
declined in most developed countries over the last 100 years. The main threats
to human health from heavy metals are associated with exposure to lead,
cadmium, mercury and arsenic (arsenic is a metalloid, but is usually classified
as a heavy metal). Emissions of heavy metals to the environment occur via a
wide range of processes and pathways, including the air (e.g. during
combustion, extraction and processing), to surface waters (via runoff and
releases from storage and transport) and to the soil and hence into ground waters
as well as crops. Atmospheric emissions tend to be of greatest concern in terms
of human health, both because of the quantities involved and the widespread
dispersion and potential for exposure that often ensues.
Cadmium – Cd
Cadmium occurs
naturally in ores together with zinc, lead and copper. Cadmium compounds are
used as stabilizers in PVC products, colour pigment, several alloys and, now
most commonly, in re-chargeable nickel– cadmium batteries. Metallic cadmium has
mostly been used as an anticorrosion agent (cadmiation). Cadmium is also present
as a pollutant in phosphate fertilizers. EU cadmium usage has decreased
considerably during the 1990s, mainly due to the gradual phase-out of cadmium
products other than Ni-Cd batteries and the implementation of more stringent EU
environmental legislation (Directive 91/338/ECC). Notwithstanding these
reductions in Europe, however, cadmium production, consumption and emissions to
the environment worldwide have increased dramatically during the 20th century.
Cadmium containing products are rarely re-cycled, but frequently dumped
together with household waste, thereby contaminating the environment,
especially if the waste is incinerated. Cigarette smoking is a major source of
cadmium exposure. Inhalation of cadmium fumes or particles can be life
threatening, and although acute pulmonary effects and deaths are uncommon,
sporadic cases still occur. Cadmium exposure may cause kidney damage. The first
sign of the renal lesion is usually a tubular dysfunction, evidenced by an
increased excretion of low molecular weight proteins [such as β2-microglobulin
and α1-microglobulin (protein HC)] or enzymes [such as
N-Acetyl-β-D-glucosaminidase (NAG)]. It has been suggested that the tubular
damage is reversible, but there is overwhelming evidence that the cadmium
induced tubular damage is indeed irreversible.
In non-smokers,
food is the most important source of cadmium exposure. Natural as well as
anthropogenic sources of cadmium, including industrial emissions and the
application of fertilizer and sewage sludge to farm land, may lead to
contamination of soils, and to increased cadmium uptake by crops and
vegetables, grown for human consumption. The uptake process of soil cadmium by
plants is enhanced at low pH. Recent research data indicate that adverse health
effects of cadmium exposure may occur at lower exposure levels than previously
anticipated, primarily in the form of kidney damage but possibly also bone
effects and fractures. Cadmium is present in most foodstuffs, but
concentrations vary greatly, and individual intake also varies considerably due
to differences in dietary habits. Women usually have lower daily cadmium
intakes, because of lower energy consumption than men. Gastrointestinal
absorption of cadmium may be influenced by nutritional factors, such as iron status.
Many individuals in Europe already exceed these exposure levels and the margin
is very narrow for large groups. Therefore, measures should be taken to reduce
cadmium exposure in the general population in order to minimize the risk of
adverse health effects.
Mercury – Hg
The chemical
element mercury is a shiny metallic liquid which occurs in only trace amounts
in igneous and sedimentary rocks. Mercury is found principally in the form of
the ore cinnabar (mercury sulfide), but can also be found in the uncombined
state. Mercury will dissolve numerous metals to form amalgams and is thus used
to extract gold dust from rocks by dissolving the gold and then boiling off the
mercury. The amalgam used in dental fillings contains tin and silver (and
sometimes gold) dissolved in mercury. The mercury compound cinnabar (HgS), was
used in pre-historic cave paintings for red colours, and metallic mercury was
known in ancient Greece where it (as well as white lead) was used as a cosmetic
to lighten the skin. In medicine, apart from the previously mentioned use of mercury as a cure for syphilis, mercury
compounds have also been used as diuretics [calomel (Hg2Cl2)],
and mercury amalgam is still used for filling teeth in many countries. Metallic
mercury is used in thermometers, barometers and instruments for measuring blood
pressure. A major use of mercury is in the chlor-alkali industry, in the
electrochemical process of manufacturing chlorine, where mercury is used as an
electrode. The largest occupational group exposed to mercury is dental care
staff. During the 1970s, air concentrations in some dental surgeries reached 20
μg/m3, but since then levels have generally fallen to about one-tenth
of those concentrations. Inorganic mercury is converted to organic compounds,
such as methyl mercury, which is very stable and accumulates in the food chain.
Until the 1970s, methyl mercury was commonly used for control of fungi on seed
grain. 
Some of the major
sources of mercury pollution include coal-fired power plants, boilers, steel
production, incinerators, and cement plants. Power plants are the largest
source, emitting around 33 tons of mercury pollution in the US annually, and contributing
to almost half of all mercury emissions. Large boilers and heaters, many of
which are powered by coal or oil, are the next largest source of mercury
emissions, followed by steel production. Incinerators are another major source.
Acute mercury
exposure may give rise to lung damage. Chronic poisoning is characterized by
neurological and psychological symptoms, such as tremor, changes in
personality, restlessness, anxiety, sleep disturbance and depression. The
symptoms are reversible after cessation of exposure. Because of the blood–brain
barrier there is no central nervous involvement related to inorganic mercury
exposure. Metallic mercury may cause kidney damage, which is reversible after
exposure has stopped. It has also been possible to detect proteinuria at
relatively low levels of occupational exposure.
Methyl mercury
poisoning has a latency of 1 month or longer after acute exposure, and the main
symptoms relate to nervous system damage. The earliest symptoms are parestesias
and numbness in the hands and feet. Later, coordination difficulties and
concentric constriction of the visual field may develop as well as auditory
symptoms. High doses may lead to death, usually 2–4 weeks after onset of
symptoms. The Minamata catastrophe in Japan in the 1950s was caused by methyl
mercury poisoning from fish contaminated by mercury discharges to the
surrounding sea. In the early 1970s, more than 10,000 persons in Iraq were
poisoned by eating bread baked from mercury-polluted grain, and several
thousand people died as a consequence of the poisoning.
The general
population is primarily exposed to mercury via food, fish being a major source
of methyl mercury exposure, and dental amalgam. Several experimental studies
have shown that mercury vapour is released from amalgam fillings, and that the
release rate may increase by chewing. Mercury in urine is primarily related to
(relatively recent) exposure to inorganic compounds, whereas blood mercury may
be used to identify exposure to methyl mercury. However, the general population
does not face a significant health risk from methyl mercury, although certain
groups with high fish consumption may attain blood levels associated with a low
risk of neurological damage to adults. Since there is a risk to the fetus in
particular, pregnant women should avoid a high intake of certain fish, such as
shark, swordfish and tuna; fish (such as pike, walleye and bass) taken from
polluted fresh waters should especially be avoided.
Lead – Pb
Lead is a
naturally occurring metal found in rock and soil and also has many industrial
applications. Due to both its natural occurrence and long history of global
use, lead is ubiquitous in the environment and is present in air, water and
soil as well as in food, drinking water and household dust. Levels of lead in
most environmental media have declined significantly over the past few decades
due to the discontinued use of lead in paint, gasoline and the solder used in
food cans. Lead has no known function in the human body. Infants and children
are most sensitive to the harmful effects of lead because they are undergoing a
period of rapid development and they absorb lead more easily and excrete it
less efficiently than adults. The most sensitive endpoint of lead toxicity in
infants and children is the reduction of intelligence quotient (IQ) score. In
adults, the strongest scientific evidence to date suggests low levels of lead
exposure may cause a small increase in blood pressure. Since the phase-out of
leaded gasoline and the subsequent reduction of airborne lead, food and drinking
water are the primary sources of lead exposure to adults within the general
population. In addition to food and drinking water, the ingestion of house dust
and soil containing lead can also significantly contribute to the lead exposure
of infants and toddlers. 
The general
population is exposed to lead from air and food in roughly equal proportions.
Earlier, lead in foodstuff originated from pots used for cooking and storage,
and lead acetate was previously used to sweeten port wine. Occupational
exposure to inorganic lead occurs in mines and smelters as well as welding of
lead painted metal, and in battery plants. Low or moderate exposure may take
place in the glass industry. High levels of air emissions may pollute areas
near lead mines and smelters. Airborne lead can be deposited on soil and water,
thus reaching humans via the food chain. Up to 50% of inhaled inorganic lead may be
absorbed in the lungs. Adults take up 10–15% of lead in food, whereas children
may absorb up to 50% via the gastrointestinal tract. Lead in blood is bound to
erythrocytes, and elimination is slow and principally via urine. Lead is
accumulated in the skeleton, and is only slowly released from this body
compartment. Half-life of lead in blood is about 1 month and in the skeleton
20–30 years.
The symptoms of
acute lead poisoning are headache, irritability, abdominal pain and various
symptoms related to the nervous system. Lead encephalopathy is characterized by
sleeplessness and restlessness. Children may be affected by behavioural
disturbances, learning and concentration difficulties. In severe cases of lead
encephalopathy, the affected person may suffer from acute psychosis, confusion
and reduced consciousness. People who have been exposed to lead for a long time
may suffer from memory deterioration, prolonged reaction time and reduced
ability to understand. Individuals with average blood lead levels under 3μmol/l
may show signs of peripheral nerve symptoms with reduced nerve conduction
velocity and reduced dermal sensibility. If the neuropathy is severe the lesion
may be permanent.
Arsenic – As
Arsenic is a
widely distributed metalloid, occurring in rock, soil, water and air. Inorganic
arsenic is present in groundwater used for drinking in several countries all
over the world (e.g. Bangladesh, Chile and China), whereas organic arsenic
compounds (such as arsenobetaine) are primarily found in fish, which may give
rise to human exposure. Smelting of non-ferrous metals and the production of
energy from fossil fuel are the two major industrial processes that lead to
arsenic contamination of air, water and soil, smelting activities being the
largest single anthropogenic source of atmospheric pollution. Other sources of
contamination are the manufacture and use of arsenical pesticides and wood
preservatives. The working group of the EU DG Environment concluded that there
were large reductions in the emissions of arsenic to air in several member
countries of the European Union in the 1980s. In 1990, the total emissions of
arsenic to the air in the member states were estimated to be 575 tons. In 1996,
the estimated total releases of arsenic to the air in the UK were 50 tons. Concentrations
in air in rural areas range from <1 to 4 ng/m3, whereas
concentrations in cities may be as high as 200 ng/m3. Much higher
concentrations (>1000 ng/m3) have been measured near industrial
sources. Water concentrations are usually <10 μg/l, although higher
concentrations may occur near anthropogenic sources. Levels in soils usually
range from 1 to 40 mg/kg, but pesticide application and waste disposal can
result in much higher concentrations.
General
population exposure to arsenic is mainly via intake of food and drinking water.
Food is the most important source, but in some areas, arsenic in drinking water
is a significant source of exposure to inorganic arsenic. Contaminated soils
such as mine-tailings are also a potential source of arsenic exposure. Absorption
of arsenic in inhaled airborne particles is highly dependent on the solubility
and the size of particles. Soluble arsenic compounds are easily absorbed from
the gastrointestinal tract. However, inorganic arsenic is extensively
methylated in humans and the metabolites are excreted in the urine. Inorganic
arsenic is acutely toxic and intake of large quantities leads to
gastrointestinal symptoms, severe disturbances of the cardiovascular and
central nervous systems, and eventually death. In survivors, bone marrow
depression, haemolysis, hepatomegaly, melanosis, polyneuropathy and
encephalopathy may be observed. Ingestion of inorganic arsenic may induce
peripheral vascular disease, which in its extreme form leads to gangrenous
changes. 
Populations
exposed to arsenic via drinking water show excess risk of mortality from lung,
bladder and kidney cancer, the risk increasing with increasing exposure. There
is also an increased risk of skin cancer and other skin lesions, such as
hyperkeratosis and pigmentation changes. Studies on various populations exposed
to arsenic by inhalation, such as smelter workers, pesticide manufacturers and
miners in many different countries consistently demonstrate an excess lung
cancer. Although all these groups are exposed to other chemicals in addition to
arsenic, there is no other common factor that could explain the findings. The
lung cancer risk increases with increasing arsenic exposure in all relevant
studies, and confounding by smoking does not explain the findings. The latest
WHO evaluation concludes that arsenic exposure via drinking water is causally
related to cancer in the lungs, kidney, bladder and skin, the last of which is
preceded by directly observable precancerous lesions. Uncertainties in the
estimation of past exposures are important when assessing the exposure–response
relationships, but it would seem that drinking water arsenic concentrations of
approximately 100μg/l have led to cancer at these sites, and that precursors of
skin cancer have been associated with levels of 50–100μg/l.
Reference:
http://large.stanford.edu/publications/coal/references/docs/167.pdf
http://www.nrdc.org/health/effects/mercury/sources.asp
http://extoxnet.orst.edu/faqs/foodcon/mercury.htm
http://www.hc-sc.gc.ca/fn-an/securit/chem-chim/environ/lead_plomb-eng.php
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